Electrocardiographic interpretation of axis deviation or prolongation of QRS assumes disease and delay or block in one or more fascicles of the ventricular conduction system (VCS). This study is based on the hypothesis that these changes in QRS may occur as a result of a number of factors in addition to disease of the VCS; and that two or more variables may occur in combination to produce the observed abnormalities in QRS. For this reason concepts which obligatorally relate most forms of QRS axis deviation and prolongation to block in one or more of the Purkinje fascicles ignore other important mechanisms and result in inappropriate clinical approaches to the problem. Preliminary observations suggest that changes in QRS axis and duration commonly referred to as complete or incomplete bundle branch block and hemiblock can occur as a result of change in any one or combination of the following variables: 1) Purkinje conduction velocity; 2) Myocardial conduction velocity; 3) Length of the conduction pathway. Axis deviation may reflect asymmetric activation of the heart. The asymmetry in depolarization may theoretically result from premature excitation of one region or delay in activation of another area. Thus, the developmental asymmetry of the VCS, asymmetric development or hypertrophy of the heart, prolongation of the circumferential- endocardial pathways, ischemia and fibrosis of the myocardium, as well as disease and block in the VCS may produce changes in QRS. This study is designed to systematically determine the significance of these various factors by correlating the characteristic surface potentials (ECG-VCG), the altered activation sequence, and the macro and micro anatomic changes in the heart. Both experimental studies in animals with acquired and congenital heart disease and observation in human subjects at the time of cardiovascular surgery will be featured. It is anticipated that this study will improve the specificity of the ECG diagnosis.